In vitro anti-inflammatory activity of spherical silver nanoparticles and monodisperse hexagonal gold nanoparticles by fruit extract of Prunus serrulata: a green synthetic approach.

Recently, green metal nanoparticles have received global attention owing to their economical synthesis, biocompatible nature, widespread biomedical and environmental applications. Current study demonstrates a sustainable approach for the green synthesis of silver nanoparticles (P-AgNPs) and gold nanoparticles (P-AuNPs) from P. serrulata fresh fruit extract. The silver and gold nanoparticles were synthesized in a very rapid, efficient and facile manner, within 50 min and 30 s at 80 °C, respectively. The nanoparticles were characterized by using visual observation, UV-Vis, FE-TEM, EDX, elemental mapping, FT-IR, XRD and DLS, which confirmed the formation of monodispersed, crystalline and stable nanoparticles. Further, we explored these nanoparticles for anti-inflammatory activity through inhibition of downstream NF-κB activation in macrophages (RAW264.7). We demonstrated that the nanoparticles reduced expression of inflammatory mediators such as nitric oxide (NO), prostaglandin E2 (PEG2), inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) was attenuated in lipopolysaccharide (LPS)-induced RAW264.7 cells. Furthermore, nanoparticles significantly suppressed LPS-induced activation of NF-κB signalling pathway via p38 MAPK in RAW 264.7 cells. To the best of our knowledge, this is the first report on the efficient green synthesis of P-AgNPs and P-AuNPs using P. serrulata fresh fruit extract and its in vitro anti-inflammatory effects. Collectively, our results suggest that P. serrulata fresh fruit extract is a green resource for the eco-friendly synthesis of P-AgNPs and P-AuNPs, which further can be utilized as a novel therapeutic agent for prevention and cure of inflammation due to their biocompatible nature.

Green synthesis of gold and silver nanoparticles using aqueous extract of Cibotium barometz root.

Green synthesis of gold (CB-AuNps) and silver (CB-AgNps) nanoparticles using Cibotium barometz root extract was highlighted. CB-AuNps were synthesized almost instantly and CB-AgNps were formed after 25 min in a heated aqueous extract. The formation of CB-AuNps and CB-AgNps was detected at 548 and 412 nm; they were spherical with crystallite sizes of 6 nm and 23 nm, respectively. CB-AgNps were further investigated for their antimicrobial activity against Escherichia, Staphylococcus aureus, Salmonella enterica, and Pseudomonas aeruginosa. Furthermore, scavenging activity against 1,1-diphenyl-2-picrylhydrzyl (DPPH) free radicals was demonstrated. Lastly, the cytotoxic properties of CB-AuNps and CB-AgNps were explored in murine macrophages (RAW264.7) cells and MCF-7 breast cancer cells. This study demonstrated the prospective biomedical applications of CB-AuNps and CB-AgNps as antioxidant, antimicrobial agents, and drug-delivery agents.

Coalescence of functional gold and monodisperse silver nanoparticles mediated by black Panax ginseng Meyer root extract.

A rapid biological synthesis of multifunctional gold nanoparticle (AuNp) and monodisperse silver nanoparticle (AgNp) was achieved by an aqueous extract of black Panax ginseng Meyer root. The physicochemical transformation into black ginseng (BG) greatly enhanced the pharmacological activities of white ginseng and its minor ginsenoside content. The optimal temperature conditions and kinetics of bioreduction were investigated. Formation of BG-AuNps and BG-AgNps was verified by ultraviolet-visible spectrophotometry at 548 and 412 nm, respectively. The biosynthesized BG-AgNps were spherical and monodisperse with narrow distribution, while BG-AuNps were icosahedral-shaped and moderately polydisperse. Synthesized nanoparticles exhibited long-term stability in buffers of pH 7.0-8.0 and biological media (5% bovine serum albumin) at an ambient temperature and at 37°C. BG-AgNps showed effective antibacterial activity against Escherichia coli and Staphylococcus aureus. BG-AuNps and BG-AgNps demonstrated increased scavenging activity against 2,2-diphenyl-1-picrylhydrazyl free radicals. In addition, BG-AuNps and BG-AgNps were nontoxic to HaCaT and MCF-7 cells; the latter showed no cytotoxicity at concentrations lower than 10 µg/mL. At higher concentrations, BG-AgNps exhibited apparent apoptotic activity in MCF-7 breast cancer cell line through reactive oxygen species generation and nuclear fragmentation.

Suppression of MAPKs/NF-κB Activation Induces Intestinal Anti-Inflammatory Action of Ginsenoside Rf in HT-29 and RAW264.7 Cells.

This study investigated the intestinal anti-inflammatory action of ginsenoside Rf in inflammatory bowel disease (IBD). IBD is a chronic inflammatory disease that affects the intestinal tract. It is associated with elevated levels of various inflammatory mediators, including interleukin (IL)-1ß, IL-6, tumor necrosis factor-α (TNF-α), nitric oxide (NO), and reactive oxygen species (ROS). Ginsenosides, the main active constituents of ginseng, have been reported to exert potent therapeutic effects against diverse diseases. However, ginsenoside Rf treatment for inflammation has not yet been examined. In this study, we evaluated the inhibitory effect of ginsenoside Rf on the inflammatory mediators downstream of p38/NF-kB activation on TNF-α-stimulated intestinal epithelial cells (HT-29) and mouse macrophage cells (RAW264.7). Our results showed that ginsenoside Rf significantly reduced the production of IL-1ß, IL-6, TNF-α, NO, and ROS, which are most highly activated in IBD. In addition, ginsenoside Rf significantly suppressed TNF-α/LPS-induced NF-κB transcriptional activity. These results suggest that ginsenoside Rf contains a compound that has potent intestinal anti-inflammatory effects that could be used to treat diseases such as IBD.

Microbial deglycosylation and ketonization of ginsenoside by Cladosporium cladosporioide and their anticancer activity.

Ginseng has been used for thousands of years in Asian countries as a traditional medicinal herb and has gained great popularity in the past decade. Ginsenosides are the major pharmacological components in ginseng. We here show that Cladosporium cladosporioide is able to convert the major ginsenoside Rb1 into four known metabolites (ginsenosides Rd, F2, CK and PPD) and two new metabolites [12ß-hydroxydammar-3-one-20(S)-O-ß-D-glucopyranoside (3-oxo-CK) and dammar-24-en-12ß,20(S)-diol-3-one (3-oxo-PPD)]. CK, PPD and 3-oxo-PPD were shown to have a potent antiproliferative activity against A549 lung cancer cells. We found that Rb1 → Rd → F2 → CK → PPD or 3-oxo-CK → 3-oxo-PPD represents the ginsenoside metabolic pathway.

Ginsenoside Rg5:Rk1 attenuates TNF-α/IFN-γ-induced production of thymus- and activation-regulated chemokine (TARC/CCL17) and LPS-induced NO production via downregulation of NF-κB/p38 MAPK/STAT1 signaling in human keratinocytes and macrophages.

Atopic dermatitis (AD) is a chronic skin disease that affects millions of people worldwide. Keratinocytes and macrophages are two cells types that play a pivotal role in the development of AD. These cells produced different chemokines and cytokines, especially thymus and activation-regulated chemokine (TARC/CCL17) and macrophage-derived chemokine (MDC/CCL22), as well as nitric oxide (NO) through inducible nitric oxide synthase (iNOS) and COX2 in response to stimulation by TNF-α/IFN-γ and lipopolysaccharide (LPS) respectively. These mediators are thought to be crucial regulators of the pathogenesis of AD. Although several natural compounds to treat AD have been studied, the effect of Rg5:Rk1 from Panax ginseng (P. ginseng) on AD has not yet been investigated. In this study, we evaluated the inhibitory effect of Rg5:Rk1 on TNF-α/IFN-γ stimulated keratinocytes (HaCaT cells) and LPS-stimulated macrophages (RAW 264.7 cells). Enzyme-linked immunosorbent assay (ELISA) data showed that pretreatment of HaCaT cells with Rg5:Rk1 significantly reduced the TNF-α/IFN-γ-induced increase in TARC/CCL17 expression in a dose-dependent manner. In addition, Rg5:Rk1 decreased LPS-mediated nitric oxide (NO) and reactive oxygen species (ROS) production in RAW 264.7 cells. A considerable reduction in messenger RNA (mRNA) expression of the aforementioned AD mediators was also observed. Pretreatment with Rg5:Rk1 attenuated the TNF-α/IFN-γ-induced phosphorylation of p38 MAPK, STAT1, and NF-κB/IKKß in HaCaT cells. Together, these findings suggest that ginsenoside Rg5:Rk1 may have a potential anti-AD effect by suppressing NF-κB/p38 MAPK/STAT1 signaling.